17 Beta-Estradiol–stimulated nitric oxide production by neutrophils: effect on platelet activation

Objective: To evaluate the effect of 17β-estradiol (E2) on the ability of human neutrophils to produce nitric oxide (NO) and its effects on platelet activation. Methods: The expression of neuronal nitric oxide synthase (nNOS) protein and the formation of NO by 17β-E2-incubated neutrophils from men w...

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Published inObstetrics and gynecology (New York. 1953) Vol. 95; no. 2; pp. 284 - 290
Main Authors Durán, Margarita G, Gálvez, Gema G, De Frutos, Trinidad, Díaz Recaséns, Joaquín, Casado, Santos, López Farré, Antonio
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.02.2000
The American College of Obstetricians and Gynecologists
Elsevier Science
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Summary:Objective: To evaluate the effect of 17β-estradiol (E2) on the ability of human neutrophils to produce nitric oxide (NO) and its effects on platelet activation. Methods: The expression of neuronal nitric oxide synthase (nNOS) protein and the formation of NO by 17β-E2-incubated neutrophils from men were studied in vitro (ten male volunteers, no medical-surgical antecedents, aged 25–45 years). Platelet aggregometry and changes in cyclic guanosine monophospate (cGMP) levels were used to bioassay the functionality of NO released from neutrophils. Results: Incubation of neutrophils derived from men with physiologic concentrations of 17β-E2 (10 −10 to 10 −8 mol/L) enhanced the expression of nNOS protein. 17β-E2-incubated neutrophils also showed a significant increase in their ability to generate NO measured by the conversion of [ 3H]- l-arginine to [ 3H]- l-citrulline. Furthermore, 17β-E2-incubated neutrophils showed a greater ability to prevent adenosine diphosphate (ADP)-induced platelet activation. Moreover, increased levels of cGMP were found in the coincubation of platelets with 17β-E2-treated neutrophils. Conclusion: These results suggest that 17β-E2 increases the ability of human neutrophils to produce NO and therefore may contribute to cardiovascular disease protection.
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ISSN:0029-7844
1873-233X
DOI:10.1016/S0029-7844(99)00567-0